华中科技大学学报（医学版）
華中科技大學學報（醫學版）
화중과기대학학보（의학판）
ACTA UNIVERSITATIS MEDICINAE TONGJI
2015年
4期
445-447
,共3页
吴志林%褚淑娟%姚尚龙%伍静
吳誌林%褚淑娟%姚尚龍%伍靜
오지림%저숙연%요상룡%오정
右美托咪定%心肌保护%缺血再灌注损伤%炎症反应
右美託咪定%心肌保護%缺血再灌註損傷%炎癥反應
우미탁미정%심기보호%결혈재관주손상%염증반응
dexmeditomidine%myocardial protection%ischemia reperfusion injury%inflammation
目的：探讨右美托咪定预处理对大鼠心肌缺血再灌注损伤以及炎症反应的影响。方法取SD大鼠40只，随机分为4组，每组10只，假手术组（Sham组）；心肌缺血再灌注组（I／R组）；常规剂量右美托咪定预处理组（Dex1组），给予右美托咪定5μg／kg负荷剂量，然后以5μg／（kg · h）持续输注1 h ，大剂量右美托咪定预处理组（Dex2组），给予右美托咪定10μg／kg负荷剂量，然后以10μg／（kg · h ）持续输注1 h。大鼠经开胸建立心肌缺血再灌注模型，以氯化三苯基四唑染色检测梗死面积，并测定血清肿瘤坏死因子α（TNF‐α）、白细胞介素6（IL‐6）、心肌组织丙二醛（MDA）、超氧化物歧化酶（SOD）的含量。结果与I／R组相比，Dex1和Dex2组炎症因子TNF‐α，IL‐6以及MDA显著降低，而SOD较I／R组显著升高（均 P＜0.05）；I／R组心肌梗死面积为（59.23±4.35）％，Dex1和Dex2组分别为（47.22±3.98）％和（48.56±4.59）％，与I／R组相比差异有统计学意义（均 P＜0.05）；Dex1组和Dex2组各指标之间差异无统计学意义（均 P＞0.05）。结论右美托咪定可通过抗氧化应激，降低炎症反应而减轻大鼠心肌缺血再灌注损伤，常规剂量即可获得一定程度的保护作用。
目的：探討右美託咪定預處理對大鼠心肌缺血再灌註損傷以及炎癥反應的影響。方法取SD大鼠40隻，隨機分為4組，每組10隻，假手術組（Sham組）；心肌缺血再灌註組（I／R組）；常規劑量右美託咪定預處理組（Dex1組），給予右美託咪定5μg／kg負荷劑量，然後以5μg／（kg · h）持續輸註1 h ，大劑量右美託咪定預處理組（Dex2組），給予右美託咪定10μg／kg負荷劑量，然後以10μg／（kg · h ）持續輸註1 h。大鼠經開胸建立心肌缺血再灌註模型，以氯化三苯基四唑染色檢測梗死麵積，併測定血清腫瘤壞死因子α（TNF‐α）、白細胞介素6（IL‐6）、心肌組織丙二醛（MDA）、超氧化物歧化酶（SOD）的含量。結果與I／R組相比，Dex1和Dex2組炎癥因子TNF‐α，IL‐6以及MDA顯著降低，而SOD較I／R組顯著升高（均 P＜0.05）；I／R組心肌梗死麵積為（59.23±4.35）％，Dex1和Dex2組分彆為（47.22±3.98）％和（48.56±4.59）％，與I／R組相比差異有統計學意義（均 P＜0.05）；Dex1組和Dex2組各指標之間差異無統計學意義（均 P＞0.05）。結論右美託咪定可通過抗氧化應激，降低炎癥反應而減輕大鼠心肌缺血再灌註損傷，常規劑量即可穫得一定程度的保護作用。
목적：탐토우미탁미정예처리대대서심기결혈재관주손상이급염증반응적영향。방법취SD대서40지，수궤분위4조，매조10지，가수술조（Sham조）；심기결혈재관주조（I／R조）；상규제량우미탁미정예처리조（Dex1조），급여우미탁미정5μg／kg부하제량，연후이5μg／（kg · h）지속수주1 h ，대제량우미탁미정예처리조（Dex2조），급여우미탁미정10μg／kg부하제량，연후이10μg／（kg · h ）지속수주1 h。대서경개흉건립심기결혈재관주모형，이록화삼분기사서염색검측경사면적，병측정혈청종류배사인자α（TNF‐α）、백세포개소6（IL‐6）、심기조직병이철（MDA）、초양화물기화매（SOD）적함량。결과여I／R조상비，Dex1화Dex2조염증인자TNF‐α，IL‐6이급MDA현저강저，이SOD교I／R조현저승고（균 P＜0.05）；I／R조심기경사면적위（59.23±4.35）％，Dex1화Dex2조분별위（47.22±3.98）％화（48.56±4.59）％，여I／R조상비차이유통계학의의（균 P＜0.05）；Dex1조화Dex2조각지표지간차이무통계학의의（균 P＞0.05）。결론우미탁미정가통과항양화응격，강저염증반응이감경대서심기결혈재관주손상，상규제량즉가획득일정정도적보호작용。
Objective To investigate the effects of different doses of dexmeditomidine pretreatment on myocardial ischemia reperfusion injury and inflammation in rats.Methods Totally 40 SD rats were randomly allocated into 4 groups (n= 10 per group):Sham group(S) ,ischemia reperfusion group(I/R) ,regular dosage of dexmeditomidine group(Dex1) ,and large dosage of dexmeditomidine group(Dex2).Continuous intravenous infusion of dexmeditomidine was given to Dex1 group at a rate of 5 μg/kg with a loading dose of 5 μg/(kg · h) for 1 h.Dosage of dexmeditomidine was doubled in group Dex2 and same dosage of saline was given to group I/R.Myocardial ischemia‐reperfusion injury model was established after the infusion.The rats were killed and sizes of myocardial infarction were measured with TTC staining method.Serum TNF‐α,IL‐6 concentration and MDA , SOD contents in myocardial tissue were analyzed.Results Serum TNF‐α,IL‐6 ,and myocardial tissue MDA were lower and SOD was higher in group Dex1 and Dex2 group than in group I/R(P< 0.05).Infarction size in group I/R was(59.23 ± 4.35)% ,which was much larger than that in group Dex1[infarction size(47.22 ± 3.98)% ]and group Dex2[infarction size (48.56 ± 4.59)% ](P<0.05).There was no difference between group Dex1 and group Dex2(P>0.05).Conclusion Dexmedi‐tomidine can relieve myocardial ischemia reperfusion injury in rats through anti‐inflammation and anti‐oxidative stress.No difference between a regular and a large dosage of dexmeditomidine in myocardial protection effect.
